Tobacco is a substance consisting of the dried leaves and stems of the plant Nicotiana tabacum which contains the addictive drug nicotine. The plant is native to North America but is now grown worldwide. Tobacco abuse has been identified as the single most preventable cause of disease, morbidity and mortality. Tobacco contains and produces many toxic chemicals and free radical species. There are three principal ways to consume tobacco: smoking, chewing and dipping and snuffing. Fifty million Americans smoke, and countless others are affected by tobacco smoke, the so-called secondary or passive smokers. Children of smokers breathe this second-hand smoke and have more respiratory problems than children of non-smokers. Non-smoking spouses and co-workers of smokers have a greater frequency of heart disease than true non-smoker controls.
Smokeless tobacco is used by as many as fourteen million individuals and has a detrimental effect on the oral cavity plus systemic effects from buccal mucosal absorption of nicotine and other injurious chemicals. There is a growing use of smokeless tobacco in adolescents and young adults. Chewing loose leaf tobacco and "dipping" moist, ground snuff tobacco are common uses of tobacco without smoking. "Snuffing" that is "snorting" dry powdered tobacco into the nasal passageways is rarely used in this country. Health risks from smokeless tobacco are still very significant and it is not a substitute for smoking. The alarming growth of use of smokeless tobacco by 10-12 year old users has brought on a massive educational campaign by the National Cancer Institute.
Because of the oro-pharynx's access to the environment, like the skin to oxygen and ultraviolet radiation, the structures of the oral cavity may be damaged by inhaled, ingested or chewed noxious substances and gaseous and particulate materials, as well as injuries by endogenous processes, such as inflammatory reactions and by drugs (xenobiotics). Reactive oxidizing species, as induced by inhaled and chewed tobacco, ozone and nitrous oxide are important factors in generating free radicals and inducing inflammatory reactions.
Leukoplakia, a tobacco induced white patch on the buccal mucosa, as found in smokers, is a localized irritation due to direct contact of smoked or smokeless tobacco and it is directly related to the frequency and years of tobacco abuse. Although leukoplakia is a benign oral lesion, it has a malignant potential, requiring a biopsy of the lesion to rule out cancer. Leukoplakia may regress or resolve completely when use of tobacco products is discontinued. Adequate oral examinations by primary physicians and dentists is paramount to reduce smoke induced mouth and tooth pathology.
Over 30,000 new cases of cancer of the oral cavity are diagnosed annually, accounting for two to four percent of all new cancers. Oral cancer kills 8,000 patients each year and only half of these cases diagnosed annually have a five year survival. The great majority of these patients are users of tobacco products. Other risk factors include alcohol abuse, nutritional deficiencies and poor oral hygiene.
In addition, tobacco contributes to other oral symptoms or pathologies of the mouth, gingiva and teeth. Tobacco may cause halitosis, may numb the taste buds, and interfere with the smell and taste of food. It may stain teeth and contribute to dental caries. Smokers have more dental tartar (calculus) than non-smokers. Tobacco is associated also with gingivitis, with severe periodontal (gum) disease and tooth loss. Acute necrotizing ulcerative gingivitis ("trench mouth") is a destructive, painful inflammatory condition occurring mainly in tobacco abusers.
Besides leukoplakia, another generalized whitish hue on the buccal mucosa represents oral submucous fibrosis. This disease occurs mainly in India and is a chronic, progressive premalignant condition. The etiology is chronic chewing of tobacco or of the areca nut or both. The fibrosis (scarring) results in restriction of mouth opening and involves the palates, tonsillar fossa, buccal mucosa and underlying muscle. Associated with this condition is also oro-pharyngeal carcinoma, with a high frequency in India and associated in 70% of cases with chewing tobacco. Smokeless tobacco and areca nut usage is also common in Pakistan, Bangladesh and Java and in these individuals and Indian immigrants to the United States and United Kingdom.
The deleterious effects of tobacco abuse are well known and regulatory agencies as well as the public constantly react to these scientific and epidemiologic evidences. Tobacco is indeed a worldwide public health hazard accounting for significant morbidity and mortality.
Cells subjected to oxidative stress resulting from the consumption of smokeless tobacco may severely affect cellular function and cause damage to membrane lipids, to proteins, to cytoskeletal structures and to DNA. Free radical damage to DNA has been measured as formation of single-strand breaks, double-strand breaks and chromosomal aberrations. Cells exposed to ionizing radiation and cigarette smoke have also been demonstrated to have an increased intracellular DNA damage, hence the frequency of oro-pharyngeal, esophageal, and pulmonary carcinomas in tobacco users.
There have been studies of the effects of smokeless tobacco on inflammation and on gingival crevicular levels of prostaglandin E2 and interleukins. Placing a quantity of smokeless tobacco on the buccal mucosa increased the levels of these molecules and there was marked inflammation as a result. It was found that the reaction in the alveolar mucosa was more severe than in the gingiva and ranged from erythema to ulceration supporting the conclusion that smokeless tobacco adversely affects periodontal tissue.
Studies have shown that Maras Powder, a type of smokeless tobacco used in Turkey, affects the micro-nuclei of buccal mucosal cells in habitual users. This provides evidence of the genotoxic effects of smokeless tobacco and its link to oral cancer. Further, it has been shown that smokeless tobacco extracts activate the complement system in in vitro tests using normal human serum. Loose leaf chewing tobacco and dry and moist snuff were studied. The studies showed that these three types of tobacco activated the complement pathway, thus it was postulated that such products provide for putative mechanisms for initiating inflammation in the oral mucosa. The inflammation reaction, in turn, generates countless free radicals which cause further damage to gingival tissues and oral mucosal cell DNA. More recently, it has been demonstrated that nicotine is cytoxic to human primary periodontal ligament and gingiva fibroblast cultures. It was thus concluded that nicotine is a definite risk factor in the progression of periodontal disease. Interestingly, epidemiological studies carried out in Sweden strongly suggest that beer and liquor consumption confer a strong risk factor for oral snuff to induce oral cancers.
The ubiquitous non-enzymatic thiol tripeptide, glutathione (GSH), plays a vital function in maintaining the integrity of the reactive oxygen species-free radical sensitive cellular components. This is accomplished through its direct role as an antioxidant, in its reduced (GSH) form, as well as a cofactor. GSH has been detected in bronchoalveolar lavage fluid. In cells, GSH is oxidized in this process to GSSG, but its cellular concentrations for antioxidant activity is maintained in equilibrium by the enzyme glutathione reductase, consuming NADPH as the source of reducing equivalents. Under states of GSH depletion, including malnutrition and severe oxidative stress, as in smoking and/or chewing tobacco, cells may become injured and die.